Sarcoid And Maxillary Sinus

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Sinonasal Wegener Granulomatosis

Fig. 6.27a,b. Wegener granulomatosis. Plain SE T1 (a) and enhanced VIBE (b) in the axial plane. On plain SE T1, relevant thickening of the mucosa lining the right maxillary sinus is seen, combined with soft tissue signal within the pterygopalatine fossa (1). b Marked enhancement of both the tissue in the pterygopalatine fossa and along the maxillary sinus walls is demonstrated. The fat suppressed sequence clearly shows the relevant enhancement of parapharyngeal spaces and nasopharyngeal walls (2). Soft tissue thickening and enhancement at the right temporomandibular joint (3) is also observed

Fig. 6.27a,b. Wegener granulomatosis. Plain SE T1 (a) and enhanced VIBE (b) in the axial plane. On plain SE T1, relevant thickening of the mucosa lining the right maxillary sinus is seen, combined with soft tissue signal within the pterygopalatine fossa (1). b Marked enhancement of both the tissue in the pterygopalatine fossa and along the maxillary sinus walls is demonstrated. The fat suppressed sequence clearly shows the relevant enhancement of parapharyngeal spaces and nasopharyngeal walls (2). Soft tissue thickening and enhancement at the right temporomandibular joint (3) is also observed b a fection, sarcoidosis, connective tissue diseases, and neoplastic lesions (basically lymphomas, metastases, and fibrous tumors) (Dalley 1999; Weber et al. 1999). In all these conditions, imaging findings should be carefully matched with clinical information and laboratory tests, as even sophisticated information provided by MR are, in itself, often insufficient to provide the diagnosis.

Neurologic manifestations of Wegener granulomatosis may be related to central/peripheral nerve involvement as well as to central nervous system localization of the disease. Cranial nerve involvement, a process triggered by small vessel vasculitides of the vasa nervorum (Drachman 1963), is rather uncommon(6.5%of cases) (Nismno et al. 1993); very rarely it has been described as the unique manifestation of the disease. MR findings include asymmetric nerve thickening, enlargement and destruction of the related foramina and fissures, and abnormal signal pattern resembling that described

Maxillary Sinuses Abnormalities
Fig. 6.28a,b. Wegener granulomatosis. SE T2 (a) and Gd-DTPA SE T1 (b) in the axial plane. Thickening of the maxillary nerve (arrows) as it courses through the pterygopalatine fossa. Note hypointense signal and mild enhancement, indicating granulo-matous tissue surrounding the nerve

in mucosal lesions and in pseudotumors (Fig. 6.28). CT is less sensitive to nerve abnormalities: actually, this technique enables the detection of late indirect signs such as pressure erosion and/or enlargement of skull base foramina and fissures.

Otologic manifestations of Wegener granu-lomatosis are related to the involvement of the Eustachian tube or of the middle ear. Active granulomatous tissue within the middle ear may exhibit enhancement differently from retained fluid observed in serous otitis media (Maroldi et al. 2001) (Fig. 6.29).

Cerebral vasculiti is rather uncommon: it may result in an intraparenchymal or subarachnoid hemorrhage, or in a stroke. The latter may also be secondary to vessel compression from mass-like pseudotumoral lesions. Remote granulomatous lesions may affect the brain parenchyma (rarely) (Provenzale and Allen 1996) or dura. Plaque thickening and marked contrast enhancement of the dura (without pial involvement) are reported, promptly responding to immunosuppressive treatment. Similar findings are detected in a list of different conditions including neurosarcoidosis, primary and secondary dural tumors, infectious diseases, hypertrophic pachymeningitis.

Destruction of central facial bone structures is the hallmark of cocaine induced midline destructive lesions. This process shows a centrifugal pattern of progression, starting from the nasal septum (eroded in 100% of patients) to involve turbinates

Midline Granulomatosis Pictures

Fig. 6.29a,b. Wegener granulomatosis. SE T1 before (a) and after (b) Gd-DTPA administration. On the right side an hy-perintense signal fills the middle ear, suggesting dehydrated fluid collection (white arrows). b On the left side, there is relevant enhancement of the retained material in the middle ear, consistent with granulation tissue (black arrows). Part of the ossicular chain is demonstrated on both sides

Fig. 6.29a,b. Wegener granulomatosis. SE T1 before (a) and after (b) Gd-DTPA administration. On the right side an hy-perintense signal fills the middle ear, suggesting dehydrated fluid collection (white arrows). b On the left side, there is relevant enhancement of the retained material in the middle ear, consistent with granulation tissue (black arrows). Part of the ossicular chain is demonstrated on both sides

Ossicular Fractures
Fig. 6.30. Cocaine induced midline destructive lesions. Gd-DTPA enhanced SE T1, axial plane. Extensive destruction of midline nasal structures with involvement of the nasal septum and both inferior turbinates. Distortion of the inferior portion of the nose is also seen
Inflamed Septum And Turbinates
Fig. 6.31. Cocaine induced midline destructive lesions. TSE T2, coronal plane. Bilateral meningoencephalocele (arrows) secondary to extensive destruction of all centrofacial structures

(inferior 75%, middle 62.5%), lateral nasal wall (medial maxillary sinus wall, lamina papyracea), both roof and floor of nasal cavities (hard and soft palate) (Fig. 6.30, 6.31). The concept of centrifugal progression is strengthened by the correlation demonstrated between the area of septal erosion and the degree of midfacial structure destruction (TriMArcHi et al. 2001).

Mucosal inflammation may also be detected on MR: signal characteristics are quite similar to those described for Wegener granulomatosis, namely T2 hypointensity combined with nonhomogeneous and decreased enhancement.

The differential diagnosis between cocaine induced midline destructive lesions and Wegener granulomatosis is rather difficult as these two entities exhibit overlapping histopathologic features and because ANCA testing may give positive results also in cocaine induced midline destructive lesions. Moreover, cocaine abusers are obviously inclined to deny drug addiction. Two elements may help to solve the diagnosis: hard and soft palate are generally spared by Wegener granulomatosis (Lloyd et al. 2002); in addition, mucosal areas with abnormal MR signal in cocaine abusers are generally confined to the septum or turbinates, where deposition of insufflated crystals occurs (TriMArcHi et al. 2001).

A very limited number of studies in the literature focus on imaging findings of sinonasal sarcoidosis - reflecting the low incidence of this condition. CT and MR findings may consist, in moderate stages, of isolated mucosal thickenings, intrasinusal air-fluid levels, and hypertrophy of turbinates, impossible to differentiate from a mere chronic sinusitis (KrESPi et al. 1995). In advanced stages, submucosal granulomas and bone erosions may be observed, shifting the differential diagnosis towards Wegener granu-lomatosis and cocaine induced midline destructive lesions. MR signal pattern of sarcoid granulomas resembles that of Wegener granulomatosis lesions (T2/T1 hypointensity, variable enhancement) (Fig. 6.32). Bone destruction may be rather extensive, both the hard and soft palate may be affected.

Actually, these three non-infectious destructive inflammatory diseases may have highly overlapping manifestations, making a CT/MR based differential diagnosis nearly impossible. The main task of imaging, therefore, is to precisely assess the extent of the lesions, particularly in deep spaces of the face.

Sarcoid The Sinuses


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Blatateral Ethmoid Disease

Fig. 6.32a-c. Sarcoidosis. TSE T2 in the coronal plane (a), fat suppressed Gd-DTPA SE T1 (b) in the axial plane, Gd-DTPA SE T1 (c) in the coronal plane; examination obtained 8 months after microendoscopic sinus surgery. A hypointense, mildly enhancing pseudomass occupies the roof of the residual ethmoid, obstructing the frontal sinus (asterisk) and encroaching the floor of anterior cranial fossa (1). Reactive changes of the adjacent dura are present (2). Bilateral thickening of infraorbital and vidian nerves (3-4); hypointense signal on T2 and vivid enhancement indicate granulomatous involvement

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